Heart failure + Hypertension Flashcards
Pathophysiology of congestive heart failure
- In a normal heart, increased ventricular filling results in increased contraction via the Frank-Starling law → increased cardiac output
- In patients with heart failure, this mechanism fails
- As the heart continues to fail → compensatory mechanisms are activated, including an increase in heart rate, catecholamine release and RAAS activation
- These mechanisms are useful in the initial period but are usually overexpressed, thus instigating a vicious cycle
- Medications such as ACE inhibitors aim to target these compensatory pathways
Common causes of congestive cardiac heart failure
- Ischaemic heart disease
- Hypertension
- Valvular disease
- Atrial fibrillation
Symptoms of left sided heart failure
- Dyspnoea: particularly exertional
- Orthopnoea and paroxysmal nocturnal dyspnoea
- Fatigue and weakness
- Cough with pink, frothy sputum
- Cardiogenic wheeze
Signs of left sided heart failure
- Tachypnoea and tachycardia
- Cool peripheries
- Peripheral or central cyanosis
- Displaced apex beat
- Stony dull percussion: if an effusion is present
- Crackles on auscultation: coarse bi-basal crackles
- Third heart sound (S3)
Symptoms of right sided heart failure
- Swelling in the legs
- Distended abdomen
- Fatigue and weakness
Signs of right sided heart failure
- Raised JVP
- Peripheral pitting oedema
- Hepatosplenomegaly
- Ascites
Which criteria is used to classify heart failure?
The New York Heart Association (NYHA) classification system
Class 1:
- no limitation of physical activity
- ordinary physical activity does not cause symptoms (fatigue, palpitation, dyspnoea)
Class 2:
- slight limitation of physical activity
- ordinary physical activity causes symptoms
Class 3:
- marked limitation of physical activity
- less than ordinary physical activity causes symptoms
Class 4:
- all physical activity causes discomfort
- symptoms at rest
Investigations for heart failure
- Bedside
- ECG: broad QRS and evidence of LVH (high amplitude)
- Bloods
- NT-proBNP:
- >400pmol/L suggests HF and requires transthoracic ECHO within 6 weeks
- >2000pmol/L requires urgent transthoracic ECHO within 2 weeks
- Acute heart failure: urgent ECHO (usually within 48 hours)
- FBC: anaemia causes high output failure
- U&Es: CKD can cause heart failure
- TFTs: hyperthyroidism can cause high output failure
- NT-proBNP:
- Imaging
- Transthoracic ECHO: assess left ventricular ejection fraction, diastolic function
- CXR: assess heart size (PA film) and evidence of pulmonary congestion
Signs of heart failure on X-ray
- A - Alveloar oedema (batwing opacities)
- B - Kerley B lines
- C - Cardiomegaly
- D - Dilated upper lobe vessels
- E - Pleural Effusion
Management of congestive heart failure
- 1st line: Beta-blocker and ACE inhibitor: start one drug at a time. Beta-blockers (e.g. bisoprolol) and ACE inhibitors (e.g. ramipril) have been shown to reduce mortality
- 2nd line: Aldosterone antagonist (e.g. spironolactone)
Congestive cardiac failure
Despite bisoprolol, ramirpil and spironolactone, the patient is breathless at rest
What is the most appropriate next step?
- Cardiac resynchronisation therapy (CRT) or implantable cardioverter-defibrillator (ICD)
- (CRT involves biventricular pacing and forces both ventricles to contract in synchrony, thereby improving cardiac output)
- (An ICD is able to perform cardioversion, defibrillation and, in some cases, pacing)
- CRT or an ICD is generally indicated in: symptomatic patients with an ECG indicating ventricular dyssynchrony (e.g. QRS >120ms) AND LVEF <35%
- Digoxin: an alternative option, particularly for patients with atrial fibrillation and heart failure due to its inotropic effects. It does not improve prognosis in patients with heart failure
- Ivabradine: an alternative option if HR >75 bpm and LVEF <35%, and the patient is already on suitable medication (e.g. bisoprolol, ramipril and spironolactone)
- Sacubitril valsartan: if LVEF <35% (will replace ACEi)
Adjunctive management of congestive heart failure
- Fluid restriction: usually limited to <1.5L/day, but varies between patients
- Loop diuretic (e.g. furosemide): confers symptomatic relief of fluid overload but no improvement in prognosis
- Annual influenza vaccine and one-off pneumococcal vaccine
Acute heart failure - key concern
Acute heart failure can cause significant pulmonary oedema and respiratory failure
Management of acute heart failure
Stabilise
- Oxygen: is SpO2 <94% or type 1 respiratory failure
- Fluid restriction: 1.5L
- IV diuretic: furosemide infusion
- Monitor daily weights and urine output
Consider
- IV nitrates: if evidence of HTN or myocardial ischaemia; reduces preload
- Inotropes (eg dobutamine): if evidence of haemodynamic instability; improves ejection fraction
- Ventilation:
- CPAP: for type 1 respiratory failure
- Mechanical ventilation if above fail
Pathophysiology of essential hypertension
Cardiac output x peripheral resistance = Mean arterial pressure
Cardiac output = Stroke volume + Heart rate
Peripheral resistance = Vascular tone (eg activation of RAAS) + Vascular structure (eg atherosclerosis)
Primary hypertension
- 90-95% of cases of hypertension
- Essential hypertension, no known underlying cause
Causes of secondary hypertension
- Renal disease
- Glomerulonephritis
- Polycystic kidney disease
- Chronic kidney disease
- Endocrine disorders
- Primary hyperaldosteronism
- Pheochromocytma
- Cushing’s syndrome
- Hyperthyroidism
- Acromegaly
- Medication
- Glucocorticoids
- Atypical antipsychotics
- Combined oral contraceptive pill
- Pregnancy
Main complications of persistent hypertension
- Brain
- Cerebrovascular accident
- Hypertensive encephalopathy
- Retina
- Hypertensive retinopathy
- Heart
- Myocardial infarction
- Hypertensive cardiomyopathy
- Kidneys
- Hypertensive nephropathy
- Hyperglycaemia
Primary investigations for hypertension
- Blood pressure
- If ≥140/90mmHg, take a second reading
- ABPM
- BP measured over a 24 hour period
- Offer to all patients with clinic BP 140/90 - 180/120
Investigations to consider:
- HBPM
- If ABPM not appropriate
Assessing risk and organ damage in hypertension
- Fundoscopy: assess for hypertensive retinopathy
- 12 lead ECG: ischaemic changes and evidence of LVH
- Albumin: creatinine ratio and urinalysis: for underlying renal dysfunction
- Bloods: HbA1c, U&Es, total cholesterol and HDL cholesterol
Assess cardiovascular risk
- QRISK: estimates risk of a myocardial infarction or stroke over thee next 10 years
Define white coat hypertension
Discrepancy of ≥20/10mmHg between the clinic reading and ABPM
What is malignant (accelerated) hypertension?
- BP ≥180/120 mmHg
- Retinal haemorrhage and/or papilloedema
- Target organ damage
Refer to emergency department
Management of hypertension: Lifestyle modification
- Improving diet
- Reducing caffeine
- Smoking cessation
- Reducing alcohol consumption
- Regular exercise
- Low salt diet (less than 6g/day, but ideally 3g/day)
Following ABPM or HBPM, which patients would you offer medication to treat hypertension?
- ≥135/85 mmHg = Stage 1 hypertension
- Treat if: <80 years AND
- Target organ disease
- Diabetes
- Establised cardiovascular disease
- Renal disease
- QRisk ≥10%
- Treat if: <80 years AND
- ≥150/95 mmHg = Stage 2 hypertension
- Treat all patients regardless of age
Target blood pressure when treated hypertension
- If <80 years old: aim for <140/90mmHg
- If >80 years old: aim for <150/90 mmHg
- If CKD: aim for <140/90mmHg
- If CKD and DM: aim for <130/80mmHg
Monotherapy options for hypertension
- Aged <55 years OR T2DM (of any age)
- Offer an ACE inhibitor (ACEi), e.g. ramipril
- If intolerant to an ACEi, such as due to a cough, offer an angiotensin receptor blocker (ARB) instead, e.g. losartan
- Aged ≥55 years OR African or Afro–Caribbean (of any age)
- Offer a calcium channel blocker (CCB), e.g. amlodipine
- If intolerant to a CCB, such as due to peripheral oedema, offer a thiazide-like diuretic instead, e.g indapamide
Second and third line management of hypertension
Second-line:
- If on an ACEi or ARB for step one: add a CCB or thiazide-like diuretic
- If on a CCB for step one: add an ACEi, ARB or thiazide diuretic
- ARBs are preferred over ACEi in African or Afro-Caribbean patients
Third-line:
- Triple therapy: combine an ACEi (or ARB) with a CCB and thiazide-like diuretic
Fourth line management of hypertension
Quadruple therapy: dependent on potassium levels. If hypertension is not controlled with 4 drugs, then consider a specialist review.
- If K+ >4.5, add an alpha- or beta-blocker
- If K+ ≤4.5, add an aldosterone antagonist such as spironolactone (a ‘K+ sparing diuretic’)
